We investigated whether the acrylamide formed during cooking carbohydrate-rich foods at high temperatures causes neoplastic changes in rat pancreas. Azaserine, which is an amino acid derivative that has the ability to initiate neoplastic changes in rat pancreas, was injected into 14-day-old male rats once a week for three weeks. Acrylamide was given to both azaserine-injected and non-injected rats at doses of 5 and 10 mg/kg/day in drinking water for 16 weeks after which tissue slides were prepared from the pancreata. Pancreas weights and body weights of rats treated with azaserine and acrylamide together increased significantly compared to the other groups. Moreover, the size, average diameter and volume of atypical acinar cell foci that developed in the pancreata of rats treated with azaserine and acrylamide together increased significantly compared to rats treated with either azaserine or acrylamide alone and control groups. Atypical acinar cell adenoma or adenocarcinoma was not observed in the pancreata of rats in any group.

We investigated short (6 months) and long (12 months) term inhibitory effects of low (200 ppm) and high (400 ppm) dosages of acetylsalicylic acid (aspirin) on exocrine pancreatic carcinogenesis. It is known that exocrine pancreatic carcinogenesis can be detected by the presence of atypical acinar cell foci (AACF) in pancreas. We investigated possible inhibitory effects of acetylsalicylic acid in an azaserine-treated rat model. AACF were produced in rats by injection with azaserine according to previous studies. Our findings showed that the number, volume and diameter of pancreatic AACF were reduced after acetylsalicylic acid application. These observations suggest that acetylsalicylic acid may exert a protective effect against neoplastic development of pancreatic acinar cells in azaserine injected rats. Our findings corroborate reports in the literature concerning the effects of aspirin in reducing neoplastic development.

The main objective of this study was to investigate the changes in free and protein-bound SH contents in methyl parathion-exposed rat tissues. The free and protein-bound SH levels are usually affected and depleted by oxidative stress-inducing agents. Results would indicate if methyl parathion toxicity partly results from depletion of sulfhydryl content of tissues. Six-week-old male Wistar albino rats were used in this study. Following exposure to methyl parathion for 3 months, the liver, the brain, and the kidney tissues were removed from the rats. The free and protein-bound SH contents were determined in these tissues. In addition, plasma lactate dehydrogenase levels were determined. Our results showed that methyl parathion exposure significantly lowers the free and protein-bound SH levels in rat tissues. However, lactate dehydrogenase activity in the blood plasma did not display any differences compared to the control group. The free SH concentrations in the control rat liver, brain, and kidney tissues were 3.78 ± 0.1 μmol/100 mg tissue, 1.56 ± 0.08 μmol/100 mg tissue, and 2.16 ± 0.08 μmol/100 mg tissue, respectively, whereas the free SH concentrations in rats exposed to methyl parathion were determined as 0.536 ± 0.1 μmol/100 mg tissue in the liver, 1.06 ± 0.1 μmol/100 mg tissue in the brain, and 0.108 ± 0.03 μmol/100 mg tissue in the kidney. The protein-bound SH concentrations in the liver and in the kidney in rats exposed to methyl parathion displayed a significant decrease also. However, the protein-bound SH level in the brain did not change significantly. These results indicate that methyl parathion exposure partially depletes the free and protein-bound SH levels. Thus, it was concluded that methyl parathion toxicity may partly result from oxidative stress.

Aim: The effect of acetylsalicylic acid (ASA) on thiol levels was studied in a rat model of azaserine carcinogenesis. Materials and Methods: ASA and azaserine were applied to the animals to research changes in cellular sulfhydryl (-SH) content and variations in free and protein-bound molecules containing the -SH group. Such effects in rats injected with azaserine were investigated at low (200 ppm) and high (400 ppm) concentrations of ASA over a relatively short (6 months) and a relatively long (12 months) period. Results: Changes in the hepatic, pancreatic, and renal -SH contents were also determined. Conclusion: Compared to the other tissues studied, the liver contained the highest levels of both free and protein-bound -SH.

Azaserine (o-diazoacetyl-L-serine) is an antimetabolite obtained from streptomycetes cultures and is used experimentally to produce atypical acinar cell focus (AACF) in rat exocrine pancreas. Propolis is a resinous hive product with antioxidant, anticarcinogenic, antimicrobial and anti-inflammatory effects that bees collect from the plants around them. In this study, we aimed performed to investigate the effect of ethanol extract of propolis (EEP) on serum biochemical changes in azaserin induced pancreatic cancer in Wistar rats. For this purpose, male Wistar albino rats were randomly divided into 4 groups, 10 in each group. AzCt and AzProp group 2-week-old male rats were given azaserine (30 mg/kg bw) intraperitoneally (ip). Propolis (EEP) (oral 80 mg/lt) was added to the drinking water of Prop and AzProp group rats. For the first time in this study, the effects of propolis on rats with neoplastic structures formed by azaserine were investigated in terms of biochemical parameters (AST, ALP, ALT, BILD, BILT, CHOL, LDH, TRIG, UREA, TAS, TOS and OSI). According to this; AzProp group values were compared to AzCt group, respectively, AST, UREA, TOS and OSI, there is a statistically significant difference in terms of values. As a result, it was seen that the oxidative stress caused by azaserine-induced neoplastic structures decreased with the use of propolis and that propolis had a positive effect on the measured biochemical parameters.